Coupling of CSF and sagittal sinus pressure in adult patients with pseudotumour cerebri

Objective Pseudotumour cerebri syndrome (PTCS including idiopathic intracranial hypertension) is characterised by the symptoms and signs of raised cerebrospinal fluid pressure (CSFp) in the absence of ventricular dilatation or an intracranial mass lesion. Its aetiology is unknown in the majority of cases but there is much evidence for impaired CSF absorption. Traditionally, sagittal sinus pressure has been considered to be independent of CSF pressure in adults. However, the discovery of stenoses of intracranial venous sinuses and introduction of venous sinus stenting has highlighted the importance of the venous drainage in PTCS. In this study, we have explored the relationship between CSFp and SSp before and during a CSF infusion test and during CSF drainage. Materials and methods Ten patients (9 females:1 male) with PTCS underwent infusion studies in parallel with direct retrograde cerebral venography. Both SSp and CSFp were recorded at a baseline and during CSFp elevation in a course of a CSF infusion test. The drainage of CSF after the CSF infusion was performed in 7 patients. In 5 cases, jugular venous pressure was also measured. Results CSFp and SSp including their amplitudes correlated significantly and strongly both at baseline (R = 0.96; p = 0.001) and during infusion (R = 0.92; p = 0.0026). During drainage, this correlation was maintained until SSp reached a stable value, whereas CSFp continued to decrease. Conclusions In this series of ten patients with PTCS, CSFp and SSp were coupled, both at baseline and during infusion. The implications of such coupling for the calculation of CSF outflow resistance are discussed.

Nonischemic cerebral venous hypertension promotes a pro-angiogenic stage through HIF-1 downstream genes and leukocyte-derived MMP-9

Cerebral venous hypertension (VH) and angiogenesis are implicated in the pathogenesis of brain arteriovenous malformation and dural arteriovenous fistulae. We studied the association of VH and angiogenesis using a mouse brain VH model. Sixty mice underwent external jugular vein and common carotid artery (CCA) anastomosis (VH model), CCA ligation, or sham dissection ( n = 20). Hypoxia-inducible factor-1α (HIF-1α), vascular endothelial growth factor (VEGF) and stromal-cell-derived factor-1α (SDF-1α) expression, and matrix metalloproteinase (MMP) activity were analyzed. We found VH animals had higher ( P < 0.05) sagittal sinus pressure (8 ± 1 mm Hg) than control groups (1 ± 1 mm Hg). Surface cerebral blood flow and mean arterial pressure did not change. Hypoxia-inducible factor-1α, VEGF, and SDF-1α expression increased ( P < 0.05). Neutrophils and MMP-9 activity increased 10-fold 1 day after surgery, gradually decreased afterward, and returned to baseline 2 weeks after surgery. Macrophages began to increase 3 days after surgery ( P < 0.05), which coincided with the changes in SDF-1α expression. Capillary density in the parasagittal cortex increased 17% compared with the controls. Our findings suggest that mild nonischemic VH results in a pro-angiogenic stage in the brain by upregulating HIF-1 and its downstream targets, VEGF and SDF-1α, increasing leukocyte infiltration and MMP-9 activity.

Changes in superior sagittal sinus pressure in children with head elevation, jugular venous compression, and PEEP

✓ Air embolism is a potential hazard during craniotomy whenever intracranial venous pressure is subatmospheric. In order to better understand both the risk of air embolism and its treatment in neurosurgical patients, the authors have investigated the relationship of superior sagittal sinus pressure (SSP) to head position in 15 children and examined the effects of both jugular venous compression and positive end-expiratory airway pressure (PEEP) on SSP. Progressive head elevation significantly decreased mean SSP and, in five patients, SSP was less than 0 mm Hg at 90° torso elevation. A PEEP of 10 cm H2O was ineffective in significantly increasing SSP at any degree of head elevation, whereas bilateral internal jugular compression always caused a significant increase in SSP. The authors conclude that children are at risk for venous air embolism when undergoing suboccipital craniectomy in the sitting position because intracranial venous pressure is often subatmospheric when the head is elevated. Furthermore, maintaining PEEP does not appear to be a reliable treatment for increasing SSP, whereas bilateral internal jugular compression is effective.

Dural posterior fossa AVM producing raised sagittal sinus pressure

✓ A patient with raised intracranial pressure secondary to a dural arteriovenous malformation (AVM) of the posterior fossa is presented. Direct shunting of arterial blood into the transverse sigmoid sinus caused a considerable increase of the sagittal sinus pressure (SSP) and elevation of intracranial pressure (ICP). Both ICP and SSP returned to normal values following obliteration of the dural AVM by selective embolization.

Pressure in the sagittal sinus during intracranial hypertension in man

✓ Intracranial pressure (ICP) and sagittal sinus pressure (SSP) were measured simultaneously in 12 patients with brain tumors and secondary intracranial hypertension (ICH). In nine, the mean SSP was largely unaffected by changes in ICP. In three, SSP changed with the ICP. In all but one patient, the ICP remained higher than SSP and, as the ICP increased, the difference between the two also increased. Sinograms performed during ICH demonstrated partial collapse of the sinuses in some patients and not in others. The mean SSP in adults with brain tumors appears to respond unpredictably to changes in ICP. Since the rate of cerebrospinal fluid drainage depends upon the gradient between ICP and SSP, intracranial spatial compensation is probably influenced by the response of SSP to ICP. Individuals with gradients that rapidly increase because their sinuses do not collapse probably compensate more rapidly than those whose sinuses do collapse. This assumed difference in the rate of spatial compensation may account for some of the variability of the ICP response to an enlarging intracranial mass or a change in cerebral blood volume.